Dynamic Alterations of Cerebral Pial Microcirculation During Experimental Subarachnoid Hemorrhage

Abstract

The study aimed to investigate the involvement of cerebral microcirculation turbulence after subarachnoid hemorrhage (SAH). Wistar rats were divided into non-SAH and SAH groups. Autologous arterial hemolysate was injected into rat's cisterna magna to induce SAH. Changes of pial microcirculation within 2 h were observed. It was found that there were no obvious changes of the diameters, flow velocity, and fluid state of microvessels in non-SAH group. With the exception of rare linear-granular flow in A4 arteriole, linear flow was observed in most of the arterioles. There was no blood agglutination in any of the arterioles. After SAH, abnormal cerebral pial microcirculation was found. Spasm of microvessels, decreased blood flow, and agglutination of red blood cells occurred. Five minutes following the induction of SAH, the diameters of the arterioles and venules significantly decreased. The decreased diameters persisted for 2 h after cisternal injection. Decreased flow velocity of venules was found from 5 to 90 min after induction of SAH. Spasm of the basilar artery and increased brain malondialdehyde were also found after SAH. We concluded that cerebral microcirculation turbulence plays an important role in the development of secondary cerebral ischemia following SAH.

Acute changes in neurovascular reactivity after subarachnoid hemorrhage in vivo

“…The few published in vivo studies investigating the cerebral microcirculation after SAH used conventional epifluorescence microscopy and were due to the limited penetration depth of this technology limited to pial vessels. [36][37][38] These vessels were of specific interest in the context of SAH since these are the only cerebral microvessels coming in direct contact with extravasated blood after subarachnoid bleeding. Indeed, pial vessels were shown to constrict after SAH in experimental animals models and in SAH patients thereby suggesting that spasms of cerebral microvessels are one of the main reasons for the cerebral ischemia observed after SAH.…”

Experimental Subarachnoid Hemorrhage Causes Early and Long-Lasting Microarterial Constriction and Microthrombosis: An in-vivo Microscopy Study

“…In analogy to SAH in humans, the endovascular model produces a vascular lesion at the skull base, which results in an immediate increase in ICP, a decrease in CPP and the selflimiting development of a hematoma due to decreasing cerebral blood flow (Bederson et al, 1995). Another technical advantage of the current study is that it is one of the few to use intravital videomicroscopy for the direct visualization of the post hemorrhagic cerebral microcirculation in vivo (Ishikawa et al, 2009;Sun et al, 2009). In comparison with previous studies which described post hemorrhagic microvasospasm ex vivo by histology on fixed tissue or by casting techniques (Ohkuma et al, 1997;Sehba et al, 2007), the current study using in-vivo microscopy has the intrinsic advantages of studying vessels in the living brain, to be able to study the whole vascular tree of the MCA, to observe dynamic changes, e.g., thrombus formation, and to uncover dynamic interactions, e.g., vasoconstriction and microthrombosis.…”

“…So far, however, most of these investigations were performed on fixed tissue (Bederson et al, 1998;Sehba et al, 1999Sehba et al, , 2005Sehba et al, , 2007 or only acutely ( < 2 hours) after SAH (Sun et al, 2009). Accordingly, little is known about the long-term spatial and temporal characteristics of post hemorrhagic microvascular constriction in the in-vivo situation.…”

Constriction and dysfunction of pial arterioles after regional hemorrhage in the subarachnoid space

“…However, this type of vasospasm cannot fully account for the occurrence of DINDs, because symptoms of cerebral ischemia can occur in patients without evidence of angiographic vasospasm (vasospasm of the large conducting cerebral arteries) (Graham et al, 1983;Pennings et al, 2004). Clinical and experimental studies have indicated that cerebral microcirculatory dysfunction is involved in the pathophysiology of DINDs after SAH (Friedrich et al, 2012 et al, 1975;Pennings et al, 2009;Pennings et al, 2004;Sun et al, 2009). Because dysfunction of the cerebral microcirculation results in cerebral ischemia after SAH, leading to poor outcomes and occasionally death, detection of the underlying mechanisms is required to improve the outcomes for SAH patients.…”